A nerve cell is a cell having an information transmission function, and its damage emerges as serious loss of a cranial nerve function. Regeneration of an axon can hardly be expected in central nerves of a brain and spinal cord, and thus, when nerve cells have damage or degeneration, activation of the nerve cells is required. A neurotrophic factor is indispensable for activation of nerve cells of central nerves and peripheral nerves such as differentiation of nerve cells, survival sustention, promotion of synapse functions, regeneration and restoration in damage of nerve cells, and the like. Among neurotrophic factors, a nervous growth factor (NGF), a brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4/5 (NT-4/5), and the like construct a neurotrophin family having 50% or more of sequence homology with a nervous growth factor (NGF) as a prototype. Activation of nerve cells is achieved by bonding a neurotrophic factor secreted outside the cells with a high-affinity receptor (Trks) to activate signal transmission through a MAP kinase (mitogen-activated protein (MAP) kinase) information transmission path that activates (phosphorylates) MAP kinases in the nerve cells, and controlling numerous genetic expressions through activation of CREB (c-AMP-response element binding protein) of a transcription factor, and the like.
Therefore, if signal transmission through a MAP kinase information transmission path can be activated, there is a possibility of clinical applications to a nervous disorder caused by degeneration of nerve cells or cellular death. Further, there is a report about a relation between brain-derived neurotrophic factors (BDNF) and some diseases. On the basis of studies using a polymorphism of a brain-derived neurotrophic factor (BDNF), there are a report that a brain-derived neurotrophic factor (BDNF) is associated with Parkinson's disease (see Non-patent Document 1), a report that a brain-derived neurotrophic factor (BDNF) is associated with Alzheimer's disease (see Non-patent Document 2), a report that a brain-derived neurotrophic factor (BDNF) is associated with depression (see Non-patent Document 3), a report that a brain-derived neurotrophic factor (BDNF) is associated with bipolar depression (see Non-patent Document 4), and a report that a brain-derived neurotrophic factor (BDNF) is associated with anxiety disorder (see Non-patent Document 5). Furthermore, there are a report that decrease in a synapse function of a genetically converted mouse having Huntington's disease is cured with administration of a brain-derived neurotrophic factor (BDNF) (see Non-patent Document 6), and a report that administration of a MAP kinase phosphorylation inhibitor provokes an antidepressant condition (see Non-patent Document 7). Accordingly, neurotrophic factors are expected to have an effect as a therapeutic agent for nervous disorders. However, since neurotrophic factors are polymer proteins, they have a problem of having difficulty in reaching the brain since they cannot pass through a blood-brain barrier even if administered from a peripheral. Thus, it has been tried to search medical drugs having a neurotrophic factor-like activity that activates nerve cells with a low-molecular weight compound and medical drugs promoting production and secretion of neurotrophic factors.
Conventionally, an agent having a neurotrophic factor-like activity containing a compound having a predetermined general formula has been proposed (Patent Documents 1 and 2). A production and secretion accelerator of a neurotrophic factor containing a compound having a predetermined general formula (see Patent Documents 3 to 5) and a nerve regeneration accelerator containing fatty acid compounds, salts thereof or prodrugs thereof (see Patent Document 6) have been proposed.
Furthermore, there has been a proposal for a pharmaceutical agent containing a compound having a predetermined general formula, which prevents and cures neurodegenerative diseases with improvement of decrease in GABAA receptor response of an astrocyte (see Patent Document 7).    Non-patent Document 1: Ann Neural. 2002 January; 51(1): 133-6    Non-patent Document 2: J Neural Transm. 2005 May; 112(5): 703-11. Epub 2004 Sep. 14    Non-patent Document 3: Neuropsychopharmacology. 2003 February; 28(2): 397-401. Epub 2002 Aug. 29    Non-patent Document 4: Br J. Psychiatry. 2006 October; 189: 317-23    Non-patent Document 5: Psychopharmacology (Berl). 2005 June; 180(1): 95-9. Epub 2005 Jan. 26    Non-patent Document 6: J. Neurosci. 2007 Apr. 18; 27(16): 4424-34    Non-patent Document 7: BIOL PSYCHIATRY 2007; 61: 661-670    Patent Document 1: Japanese Unexamined Patent Application (JP-A) No. 2000-7568    Patent Document 2: JP-A No. 2003-113085    Patent Document 3: JP-A No. 2002-80467    Patent Document 4: JP-A No. 2003-261545    Patent Document 5: WO No. 2003/084542    Patent Document 6: WO No. 2005/032535    Patent Document 7: JP-A No. H07-316092